Rheumatoid Arthritis is a chronic inflammatory autoimmune disease that involves the joints and may cause systemic manifestations.
It is an autoimmune disease with unknown causes and contributing factors (genetic & environmental factors). Environmental factors like viral infections and cigarette smoking; trigger and maintain joint inflammation.
- Prevalence; 1% worldwide
- Gender; Women:Men = 3:1 (after 50 years old, gender difference is less marked)
- Age; peaks at 35-45 years old, although it can occur at any age – when it occurs in childhood, it is called “Juvenile Idiopathic Arthritis”
- Limitations of activities: * 33% have major activities limited * 29% cannot perform major activities
Rheumatoid arthritis pathophysiology is shown in the map in the form of a cascade process that starts with an “Autoimmune Reaction” and ends with “Joint Destruction.”
Nonspecific signs & symptoms (for weeks/months): fever, malaise, arthralgias, and weakness.
Specific signs and symptoms that take weeks to months to appear.
Joint symptoms are characteristically symmetric, including:
- Stiffness lasts > 60 minutes after rising in the morning but may occur after any prolonged inactivity (called gelling).-
- Erythema, warmth, swelling, and limitation of motion.
Joints involved in rheumatoid arthritis
- The most common joints involved are; Wrists, feet (MTP), and the index (2nd) and middle (3rd) metacarpophalangeal (MCP) joints
- Other joints include; Proximal interphalangeal (PIP) joints, shoulders, elbows, hips, knees, and ankles.
- Any joint, except the distal interphalangeal (DIP) joints.
Irreversible joint deformities that may occur due to disease progression
- Ulnar deviation of the fingers
- Boutonniere Deformity (hyperextension of the DIP & flexion of the PIP joint)
- Swan Neck Deformity (hyperextension of the PIP & flexion of the DIP joint)
- Hammer toe deformity
The disease progresses most rapidly during the first 6 years, particularly the first year; 80% of patients develop some permanent joint abnormalities within 10 years.
Most of rheumatoid arthritis extra-articular manifestations are collected in this image:
This part of the map includes History and Examination, Laboratory tests, Radiographic test (x-ray), ACR Rheumatoid Arthritis Diagnostic Criteria (2010). In addition, a comparison between rheumatoid arthritis and osteoarthritis is included.
Medications to Reduce Pain and Inflammation
1) Non-Steroidal Anti-inflammatory Drugs (NSAIDs)
- e.g., ibuprofen, naproxen, ketoprofen, piroxicam, and diclofenac.
- adjunctive therapy.
- treat symptoms and decrease inflammation but do not affect disease progression.
- dose can be decreased or discontinued with successful Disease-modifying antirheumatic drugs (DMARDs) therapy.
- adverse effects: GI toxicity, headache, confusion, and other CNS symptoms, increased BP, worsening of hypertension, edema, and decreased platelet function. NSAIDs increase cardiovascular risk.
- Non-steroidal anti-inflammatory drug drugs mechanism of action is shown in this diagram:
2) COX-2 inhibitor (only celecoxib)
See the map.
3) Low-dose systemic corticosteroids (CS)
- adjunctive therapy
- decrease inflammation and other symptoms rapidly and efficiently
- slow bone erosion
When to use low-dose systemic CS in RA?
- In early RA, low-dose oral prednisone (<10 mg/day) in combination with DMARDs for up to 6 months, as symptomatic effects ↓ with time
- In established RA, CS may be used as ‘bridging’ therapy when DMARDs are initiated, and should be withdrawn once DMARDs have controlled the disease
- May be used for severe joint or systemic manifestations of RA (eg, vasculitis, pleurisy, pericarditis)
- Relative contraindications include PUD, HTN, untreated infections, DM, and glaucoma
- The risk of latent TB should be considered before CS therapy is begun
4) Intraarticular depot corticosteroids
- Temporarily control severe monarticular or even oligoarticular symptoms.
- Triamcinolone hexacetonide may suppress inflammation for the longest time.
- Triamcinolone acetonide and methylprednisolone acetate are also effective.
- No single joint should be injected with a corticosteroid more than 3 to 4 times a year, as too-frequent injections may accelerate joint destruction.
- Because injectable corticosteroid esters are crystalline, local inflammation transiently increases within a few hours in < 2% of patients receiving injections.
- Although infection occurs in only < 1:40,000 patients, it must be considered if pain occurs > 24 h after injection.
Medications to Prevent Disease Progression & Loss of Joint Function
1) Disease-modifying antirheumatic drugs (DMARDs)
Also called “nonbiologic DMARDs,” include: methotrexate (MTX), hydroxychloroquine (HCQ), azathioprine (AZA), sulfasalazine (SSZ), and leflunomide. Other available but rarely used DMARDs include minocycline, azathioprine, cyclosporine, and tacrolimus.
- Early treatment of RA (< 6 months after the onset of symptoms) with DMARDs retard disease progression more efficiently and induce more remissions.
- Until the full action of DMARDs takes effect, anti-inflammatory or analgesic medications may be required as bridging therapy to reduce pain and swelling.
- They differ from each other chemically and pharmacologically.
- Patients should be informed about the risks of DMARDs and monitored closely for evidence of toxicity.
- Combinations of DMARDs may be more effective than single drugs. Also, combining a DMARD with another drug, such as methotrexate plus a TNF-α antagonist or an IL-1 receptor antagonist or a rapidly tapered corticosteroid, may be more effective than using DMARDs alone.
A comparison between DMARDs is available in the map. The comparison is showing: mechanisms of actions, indications, doses, adverse effects, monitoring parameters, and contraindications.
2) Biologic agents
- Also called “biologic DMARDs.”
- They are not given in combination with each other due to increased frequency of infections.
- Approved by the FDA to treat moderate to severe RA not responded to an one or more of the traditional DMARDs.
- They may be used alone, but are often in combination with other DMARDs, to increase the efficacy and decrease AE.
- Start biologic agents while patients remain on NSAID and/or corticosteroid.
A comparison between the biologic agents is available in the map. The comparison is showing: mechanisms of actions, indications, doses, onset of action, adverse effects, contraindications, and warnings/cautions.
3) Other immunomodulatory, cytotoxic, and immunosuppressive drugs
e.g., Azathioprine, and cyclosporin A. Rarely cyclophosphamide and d-Penicillamine.
- Efficacy is similar to DMARDs but more toxic.
- Used in case of treatment failure with DMARDs or to decrease the need for CSs.
- Used infrequently unless there are extra-articular complications.
And here is a comparison between them:
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